It has been demonstrated that the most important load compensation mechanisms are the force-length and force-velocity relationships of the diaphragm and two neural reflexes which increase respiratory drive. These are the vagally-dependent prolongation of inspiration which allows an increase in the peak integrated activity of the phrenic nerve and the external intercostal muscles, and the progressive increase in peripheral chemoreceptor stimuli. Although a number of studies have examined the effects of anesthesia in man and in animals on the responses to mechanical loads, these studies have their limitations. They include the failure to examine the effects of clinically relevant inhalational anesthetics (halothane, enflurane and isoflurane) and the absence of neurophysiological studies on the effects of general anesthetics on the load adjustment mechanisms or on the effects of inhalational anesthetics on the responses to CO2 and hypoxemia. The proposed studies will examine and compare the effects of halothane, enflurane and isoflurane in cats on mechanical load compensation and responses to chemical stimuli. The studies will measure the tidal volume, airway pressure, respiratory timing, and neural reflex responses to single breath and to continuous inspiratory elastic loads and to tracheal occlusion applied to FRC, and also these responses to CO2 and to hypoxemia. The effects of bilateral cervical vagotomy will also be examined. The data will be compared to the investigator's pre-existent data and concurrent studies on cats anesthetized with chloralose and urethan. Further, neurophysiological analysis will examine the effects of inhalational anesthetics on the pattern of discharge of the phrenic neurogram and external intercostal myogram.